liver part 1 cont. Flashcards
clinical features of portal vein Obstruction and Thrombosis
- Abdominal pain
- Ascites
- Oesophageal Varices
- Acute impairment of visceral blood flow –>
Congestion and Bowel Infarction
cause of Portal Vein Obstruction and Thrombosis
Impaired Blood Flow
Into the Liver
casue of Impaired blood flow Troughthe liver
– Cirrhosis (most common intra-hepatic cause)
– Sickle Cell disease: Obstruction of the sinusoids
by sickled red cells –> Pan-lobular parenchymal
necrosis
– Disseminated Intravascular Coagulation (DIC) –>
Occlusion of sinusoids
casue of Passive Congestion &
Centri-Lobular Necrosis
Systemic circulatory disorders:
* Right-sided cardiac Decompensation –> Passive
Congestion of the Liver
* Long-standing cases –> Centri-Lobular necrosis
and peri-venular fibrosis in the necrotic areas
Laboratory findings:
– Mild elevation of serum transaminase levels
– Hyper-bilirubinaemia and elevated alkaline
phosphatase (some cases)
Findings of what type of Condition?
Passive Congestion &
Centri-Lobular Necrosis
Macroscopic features:
– Slightly enlarged
– Tense
– Cyanotic Liver
Microscopic findings:
– Congestion of Centri-Lobular sinusoids
– Atrophic Centri-Lobular Hepatocytes –> Markedly attenuated Liver cell cords
– In continuous chronic severe Congestive Heart Failure
–> “Cardiac Sclerosis” or “Cardiac Cirrhosis”:
Mainly, development of centri-lobular fibrosis, with rarely formation of bridging fibrous septa and Cirrhosis
Features of what type of condition?
Passive Congestion & Centri-Lobular Necrosis casued by Right-sided Cardiac Failure
Macroscopic picture:
– Variegated mottled appearance, with Centri-Lobular
localised areas of haemorrhage and necrosis,
alternating with pale mid-zonal areas –> “Nutmeg”
liver
-Centri-lobular region is suffused with red blood cells
Centri-Lobular Haemorrhagic
Necrosis (Nutmeg Liver) –> casued by Left-sided hypo-perfusion + Right-sided retrograde congestion
cause of Hepatic vein Thrombosis aka Budd-Chiari Syndrome
Polycythaemia Vera, Pregnancy, use of Oral Contraceptives, Paroxysmal Nocturnal
Haemoglobinuria, Hepatocellular Carcinoma; 10% of
cases idiopathic
Clinical features of Hepatic Vein Thrombosis akaBudd-Chiari Syndrome
– Hepatomegaly
– Ascites
– Abdominal pain
Macroscopic features:
– Swollen and red-purple liver
– Tense organ capsule
Microscopic findings:
– Severe Centri-Lobular congestion and necrosis
– Centri-Lobular fibrosis (when Thrombosis develops
more slowly)
– Completely or incompletely occlusive fresh Thrombi in the lumen of Major Veins
– Organised adherent Thrombi (chronic cases)
Features of what type of Condition?
Hepatic Vein Thrombosis
Treatment of Hepatic vein Thrombosis
- Surgical creation of porto-systemic venous shunt
– Angiography for direct dilation of Vena Cava
obstruction
patho of Hepatic Vein Thrombosis
– Majority of the conditions –> Thrombotic
tendencies
– Hepatocellular Carcinoma –> Hyper-coagulability
state (sluggish blood flow)
– Massive intrahepatic Abscess or Parasitic Cyst –>
Mechanical obstruction to blood outflow
– Thrombus or Tumour –> Obstruction of the
inferior Vena Cava, at the level of the Hepatic
Veins
cause of Sinusoidal Obstruction Syndrome
aka Veno-Occlusive Disease
Chemotherapeutic agents (e.g. Cyclo-Phosphamide, Actinomycin D, and Mithramycin), and total body
radiation (used in pre- or post-transplantation regimens)
patho of Veno-Occlusive Disease (Sinusoidal Obstruction Syndrome)
– Toxic injury to sinusoidal endothelium causes:
–> Sloughing of damaged endothelial cells –> Formation of Thrombi–> Obstruction of sinusoidal flow –> Leak of erythrocytes into the space of Disse
–> Proliferation of stellate cells and fibrosis of the
terminal branches of the Hepatic Vein
Clinical presentations of Sinusoidal Obstructive Syndrome
– Onset, in the first 20 to 30 days after bone
marrow transplantation (20% of recipients)
– Resemblance to Budd-Chiari Syndrome, ranging from mild to severe forms
casues of Fluminant Hepatic Failure
Viral Hepatitis (HCV > HBV)
Macroscopic features:
– Shrinkage of Liver due to massive loss of mass (500-
700gr)
– Limp, red organ
– Wrinkled, large capsule
– Cut surface of necrotic areas: Muddy red mushy appearance with haemorrhage
Microscopic findings:
– Complete destruction of Hepatocytes in neighbouring lobules –> Collapsed reticulin framework and preserved portal tracts
– Little inflammatory reaction, except in cases of survival –> Massive accumulation of inflammatory cells
Are the features of what type of Syndrome
Fulminant Hepatic Failure
cause of Focal Nodualr Hyperplasia
Long-term use of Anabolic Hormones or of Contraceptives
Epi of focal Nodular Hyperplasias
Young to middle-aged adults
Macroscopic features:
* Well-demarcated but poorly encapsulated nodule
* Lighter colouration than the surrounding Liver
* *Central gray-white, depressed stellate scar, with radiations to the periphery
Microscopic findings:
* Large arterial vessels within central scar, showing
fibro-muscular hyperplasia and narrowing of their lumen
* Foci of intense lymphocytic infiltrates within the radiating septa
* Marked bile duct proliferation along septal
margins
* Normal appearing Hepatocytes in the parenchymabetween the septa, but with a thickened plate architecture (typical for regeneration)
Are the features of what type of Condition
Focal Nodular Hyperplasia
Macroscopic features:
* Entirely transformed Liver into roughly sphaerical nodules, in the absence of fibrosis
Microscopic findings:
* Plump hepatocytes surrounded by rims of atrophic Hepatocytes (reticulin stain)
Are the features of what type of Condition?
Nodular Regenerative Hyperplasia
complications of Nodular Regenerative Hyperplasia
Portal Hypertension
loc. of Cavernous Haemangiomas
Directly beneath the capsule
Epi of Cavernous Haemangiomas
Most common benign Liver Tumours
